Increased activation of RAAS may have a key role in the development and maintenance in AF. Especially angiotensin II and aldosterone draw attention. Aldosterone has hypertensive action, induces hypertrophy and fibrosis of cardiomyocytes and endothelium, modulating ion currents and refractoriness in the heart cycle. Arrhythmogenic aldosterone mechanisms include inhibition of noradrenalin reuptake, attenuation of baroreceptor activity, increase their sensitivity to catecholamines and reduce sinus rhythm variability. The expression of both the aldosterone receptor and angiotensin II receptors (AT1 and AT2) is increased in the atria of AF patients. For example, Boldt et al. reported a 100 % increase in AT1 receptor density in the left atrium in patients with chronic and paroxysmal AF compared to sinus rhythm . This reflects increased tissue activation of angiotensin II in fibrillating atria. Moreover, multiple studies have demonstrated a vicious cycle of RAAS in which aldosterone enhances the effects of angiotensin II, in part via an increased transcription of the AT1 receptor, whereas angiotensin II increases systemic and tissue levels of aldosterone. These findings are consistent with findings of elevated plasma levels of both angiotensin II and aldosterone during AF in a study by Goette et al. By blocking mineralocorticoid receptors with MRAs, RAAS over-activation can be diminished. Available data suggest that there are direct effects of spironolactone on the structural and electrical properties of the atria, preventing occurrence and maintenance of AF through its antifibrotic properties, as well as the indirect influence of improved control of heart failure and hypertension, both of which are known risk factors for AF.